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Related Concept Videos

Overview of Cell Death01:30

Overview of Cell Death

5.6K
Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
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The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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Apoptosis01:30

Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Necrosis01:16

Necrosis

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Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
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Autophagic Cell Death01:18

Autophagic Cell Death

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Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
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Author Spotlight: THP-1 Macrophage Response to LPS/ATP &#8212; Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
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Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum

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How Cells Die in Psoriasis?

Chung-Han Chen1, Nan-Lin Wu2,3,4, Tsen-Fang Tsai5

  • 1Department of Education, National Taiwan University Hospital, Taipei City 100, Taiwan.

International Journal of Molecular Sciences
|May 7, 2025
PubMed
Summary
This summary is machine-generated.

Psoriasis involves multiple programmed cell death pathways, including autophagy, necroptosis, pyroptosis, and ferroptosis. Understanding these mechanisms offers new therapeutic targets for effective psoriasis treatment.

Keywords:
cell deathprospective therapeutic approachespsoriasis

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Area of Science:

  • Dermatology
  • Immunology
  • Cell Biology

Background:

  • Psoriasis is a chronic, immune-mediated skin disease.
  • It features keratinocyte hyperproliferation and inflammation.
  • Multiple programmed cell death pathways contribute to its pathogenesis.

Purpose of the Study:

  • To review and analyze diverse cell death modes in psoriasis.
  • Focus on keratinocyte cell death patterns and molecular signatures.
  • Identify therapeutic targets based on cell death mechanisms.

Main Methods:

  • Literature review following Nomenclature Committee on Cell Death guidelines.
  • Analysis of psoriatic lesions for distinct cell death mechanisms.
  • Examination of molecular signatures and signaling pathways.

Main Results:

  • Identified autophagy dysfunction (IL-17A), decreased apoptosis, anoikis, upregulated necroptosis (RIPK1/MLKL), pyroptosis (gasdermin), PANoptosis, parthanatos (PARP1), ferroptosis, cuproptosis, and NETosis.
  • Correlations found between ferroptosis and Th22/Th17 responses.
  • NETosis linked to Th17 axis amplification.

Conclusions:

  • The interplay of various cell death pathways is crucial in psoriasis.
  • Targeted therapies (mTOR inhibitors, RIPK1 inhibitors, ferroptosis/NETosis modulators) show promise.
  • These strategies offer new directions for psoriasis treatment.